The central hypothesis of this pilot and feasibility application is that partial bladder outlet obstruction results in changes in intracellular calcium sequestration mechanisms in smooth muscle of the bladder wall, leading to hypertophy. Damage to the sarcoplasmic reticulum produces a sustained rise in cytosolic calcium and activates the calcineurin pathway. Elevated basal cytosolic Ca 2+ activates calcineurin's phosphatase activity, enabling it to dephosphorylate the nuclear factor of activated T-cells (NFAT), which can then cross the nuclear membrane to function as a transcription factor. Cyclosporin A (CSA) blocks calcineurin activity and serves as a pharmacologic probe for the contribution of this pathway to the pathophysiology of bladder wall hypertrophy. Our preliminary data suggest that the calcineurin pathway is activated in response to partial bladder outlet obstruction and accounts for part of the resulting bladder wall hypertrophy.